ArticleCardiovascular research2013
Chronic myocardial infarction promotes atrial action potential alternans, afterdepolarizations, and fibrillation.
Article in Cardiovascular research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 43 citations in OpenAlex.
- Integrative human atrial modelling unravels interactive protein kinase A and Ca2+/calmodulin-dependent protein kinase II signalling as key determinants of atrial arrhythmogenesis.Cardiovascular research · 2023Article
- Mechanisms of spontaneous CaThe Journal of physiology · 2023Article
- Adrenoceptor sub-type involvement in CaPflugers Archiv : European journal of physiology · 2022Article
- Dynamic but discordant alterations in zDHHC5 expression and palmitoylation of its substrates in cardiac pathologies.Frontiers in physiology · 2022Article
- Implications of new-onset atrial fibrillation on in-hospital and long-term prognosis of patients with acute myocardial infarction: A report from the CBD bank study.Frontiers in cardiovascular medicine · 2022Article
- ESC working group on cardiac cellular electrophysiology position paper: relevance, opportunities, and limitations of experimental models for cardiac electrophysiology research.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2021Review
- The role of basement membranes in cardiac biology and disease.Bioscience reports · 2021Review
- RyR2 and Calcium Release in Heart Failure.Frontiers in physiology · 2021Review
- Resiniferatoxin reduces cardiac sympathetic nerve activation to exert a cardioprotective effect during myocardial infarction.International journal of clinical and experimental pathology · 2021Article
- Heart failure-induced atrial remodelling promotes electrical and conduction alternans.PLoS computational biology · 2020Article
- Characterization of a porcine model of atrial arrhythmogenicity in the context of ischaemic heart failure.PloS one · 2020Article
- Dynamic clamping human and rabbit atrial calcium current: narrowing IThe Journal of physiology · 2019Article
- Increased thin filament activation enhances alternans in human chronic atrial fibrillation.American journal of physiology. Heart and circulatory physiology · 2018Article
- Impact of Renal Denervation on Atrial Arrhythmogenic Substrate in Ischemic Model of Heart Failure.Journal of the American Heart Association · 2018Article
- Profibrotic, Electrical, and Calcium-Handling Remodeling of the Atria in Heart Failure Patients With and Without Atrial Fibrillation.Frontiers in physiology · 2018Article
- Aerobic Interval Training Prevents Age-Dependent Vulnerability to Atrial Fibrillation in Rodents.Frontiers in physiology · 2018Article
- Description of the Human Atrial Action Potential Derived From a Single, Congruent Data Source: Novel Computational Models for Integrated Experimental-Numerical Study of Atrial Arrhythmia Mechanisms.Frontiers in physiology · 2018Article
- Calcium in the Pathophysiology of Atrial Fibrillation and Heart Failure.Frontiers in physiology · 2018Review
- Shensong Yangxin capsule reduces atrial fibrillation susceptibility by inhibiting atrial fibrosis in rats with post-myocardial infarction heart failure.Drug design, development and therapy · 2018Article
- CaAmerican journal of physiology. Heart and circulatory physiology · 2017Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
aimsAtrial fibrillation (AF) is increased in patients with heart failure resulting from myocardial infarction (MI). We aimed to determine the effects of chronic ventricular MI in rabbits on the susceptibility to AF, and underlying atrial electrophysiological and Ca(2+)-handling mechanisms. METHODS AND
resultsIn Langendorff-perfused rabbit hearts, under β-adrenergic stimulation with isoproterenol (ISO; 1 µM), 8 weeks MI decreased AF threshold, indicating increased AF susceptibility. This was associated with increased atrial action potential duration (APD)-alternans at 90% repolarization, by 147%, and no significant change in the mean APD or atrial global conduction velocity (CV; n = 6-13 non-MI hearts, 5-12 MI). In atrial isolated myocytes, also under β-stimulation, L-type Ca(2+) current (I(CaL)) density and intracellular Ca(2+)-transient amplitude were decreased by MI, by 35 and 41%, respectively, and the frequency of spontaneous depolarizations (SDs) was substantially increased. MI increased atrial myocyte size and capacity, and markedly decreased transverse-tubule density. In non-MI hearts perfused with ISO, the I(CaL)-blocker nifedipine, at a concentration (0.02 µM) causing an equivalent I(CaL) reduction (35%) to that from the MI, did not affect AF susceptibility, and decreased APD.
conclusionChronic MI in rabbits remodels atrial structure, electrophysiology, and intracellular Ca(2+) handling. Increased susceptibility to AF by MI, under β-adrenergic stimulation, may result from associated production of atrial APD alternans and SDs, since steady-state APD and global CV were unchanged under these conditions, and may be unrelated to the associated reduction in whole-cell ICaL. Future studies may clarify potential contributions of local conduction changes, and cellular and subcellular mechanisms of alternans, to the increased AF susceptibility.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.